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Biomedical subjects

Y Yui

Publications and source records attributed to Y Yui.

At least 91 records · Page 5Linked to original sources
PubMed1988

Effects of thermal denaturation on the longitudinal relaxation time (T1) of water protons in protein solutions: study of the factors determining the T1 of water protons.

The factors determining the longitudinal relaxation time (T1) of water protons in protein solutions were investigated by analyzing the effects of thermal denaturation on the T1 of the water protons. We treated the water protons and the protein protons "on a protein surface" as a dipole-dipole coupled two-spin system where relative translational diffusion is the dominant mechanism, and measured the change in the time development of the nuclear Overhauser effect (NOE) factors of the water protons. The T1 of the water protons was shortened markedly when the proteins were thermally denatured. Our analysis indicates that this relaxation enhancement is due to an increase in the value of the translational correlation time as well as the fraction of hydration water molecules, though the influence of "proton exchange" between the water protons and the labile protein protons cannot be completely neglected.

Animals↗
PubMed1988

Effect of deuterium oxide on leukotriene C4 generation in immunologically stimulated human leukocytes.

Addition of deuterium oxide (D2O), 6-36%, resulted in a dose-dependent increase in allergen- or anti-IgE-induced leukotriene C4 (LTC4) generation from human basophils. In the presence of 36% D2O, the enhancement was 260 +/- 135% for allergen stimulation and 480 +/- 152% for anti-IgE stimulation as compared with the control incubated in normal buffer. The increasing effect of D2O on LTC4 generation from basophils was completely reversed by washing the cells before incubation with allergen. Vinblastine as well as colchicine, at a concentration of 100 microM, counteracted the effect of D2O. The enhanced release of histamine and LTC4 from basophils challenged with allergen was suppressed by Dimaprit, a histamine H2 receptor agonist, at a concentration required to inhibit the release by 50% of 5 X 10(-5) M for histamine and 10(-5) M for LTC4. These observations suggest that microtubules may be involved in LTC4 generation from immunologically stimulated basophils.

Basophils↗
PubMed1988

Serum prostacyclin stabilizing factor is identical to apolipoprotein A-I (Apo A-I). A novel function of Apo A-I.

Serum PGI2 stabilizing factor (PSF) was purified from human serum to a single protein with a molecular weight of 28,000 D by SDS-PAGE. Analyses of NH2-terminal sequence (32 residues), COOH-terminal sequence (3 residues) and the composition of amino acids disclosed its homology with human apolipoprotein A-I (Apo A-I), a major apolipoprotein of HDL. Apolipoprotein A-II, C-I, C-II, C-III, D and E, as well as LDL, and VLDL did not possess this activity. The alpha-helix structure of Apo A-I is necessary for the binding of PGI2. HDL and nascent HDL reconstituted from Apo A-I and phospholipid significantly prolonged the half-life of PGI2. PGI2 stabilization by HDL and Apo A-I may be an important protective action against the accumulation of platelet thrombi at sites of vascular damage. The beneficial effect of HDL in the prevention of coronary artery disease may be partly due to this action.

Amino Acid Sequence↗
PubMed1988

Platelet aggregation and thromboxane B2 release in patients with acute myocardial infarction--their relation to coronary patency.

Platelet function in the aortic blood in 39 patients who underwent intracoronary thrombolysis with urokinase was evaluated in the acute stage of myocardial infarction and after 4 weeks. The patients were classified into 2 groups according to the patency of the infarct vessel shown by coronary arteriography before urokinase administration. In the acute stage, 26 patients with completely occluded infarct vessel (group 1) showed a decreased level of platelet aggregation induced by adenosine diphosphate or arachidonic acid as compared with 13 patients with patent infarct vessel (group 2). The platelet aggregation in group 1 increased 4 weeks later and both groups showed similarly enhanced platelet aggregation levels as compared with normal controls. Like platelet aggregation, serum thromboxane B2 production in group 1 was lower than that in group 2 in the acute stage. Plasma thromboxane B2 levels in the aorta in both groups were significantly elevated in the acute stage, and were normalized after 4 weeks. This elevation of thromboxane B2 seems to be due to its washout from the infarct vessel, because plasma thromboxane B2 levels were significantly higher in the great cardiac vein than those in the aorta after successful reperfusion in group 1 or group 2. In conclusion, despite a significant elevation in plasma thromboxane B2 levels, platelet aggregation and serum thromboxane B2 production relatively decrease in patients with totally occluded infarct vessel. The patency of the infarct vessels should be taken into account when evaluating platelet function in acute myocardial infarction.

Adult↗
PubMed1988

Reocclusion of the infarcted vessel during acute interventions in myocardial infarction.

Acute reocclusion of the recanalized infarcted vessel was observed during thrombolytic therapy in 28 or 138 patients, and during angioplasty following thrombolysis in 5 of 70 patients. The occluded vessel reopened again in 20 of 28 patients by additional administration in nitroglycerin and urokinase and in 3 of 5 patients by repeated angioplasty. There was no significant difference in success rate of thrombolysis or angioplasty between patients with acute reocclusion and those without. However, reinfarction after acute intervention tended to be more common in the former patients than the latters.

Aged↗
PubMed1988

Enhancement of coronary thrombolysis with plasminogen pro-activator by pretreatment with heparin.

The effect of pretreatment with heparin on coronary thrombolysis by plasminogen pro-activator was studied in 20 dogs with a 1-h old clot in the left anterior descending coronary artery. The clot was induced by placement of a copper coil and thrombolysis was confirmed angiographically. Intravenous administration of plasminogen pro-activator at a rate of 5 micrograms/kg/min (group 1; n = 5) and 20 micrograms/kg/min (group 2; n = 5) after pretreatment with heparin (300 IU/kg) induced thrombolysis in 31 +/- 4 min and 14 +/- 2 min, respectively. When plasminogen pro-activator was administrated intravenously at a rate of 20 micrograms/kg/min without heparin pretreatment (group 3; n = 5), the infusion interval for successful thrombolysis was prolonged to 45 +/- 6 min, which was significantly longer than that in groups 1 and 2 (p less than 0.001). In these three treatment groups, thrombolysis was not associated with severe alteration in plasma hemostatic factors (fibrinogen and alpha 2-antiplasmin). An evaluation of plasma urokinase activities using a chromogenic substrate S-2444 did not show that heparin increased the plasma urokinase activities. By increasing the dose of plasminogen pro-activities. By increasing the dose of plasminogen pro-activator to 80 micrograms/kg/min, successful reperfusion was rapidly obtained in 25 +/- 5 min without heparin pretreatment (group 4; n = 5); this was significantly faster than the results seen in group 3 (p less than 0.001). An analysis of urokinase activities showed that plasminogen pro-activator was fully converted to urokinase, which induced complete depletion of fibrinogen and alpha 2-antiplasmin.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1987

Enhancement of IgE synthesis and histamine release by T cell factors derived from atopic patients with bronchial asthma.

Culture supernatants of unstimulated T cells (TCS) derived from normal donors or from atopic patients with bronchial asthma were tested for their ability to regulate the spontaneous IgE synthesis by B cells of normal and atopic subjects. The same TCS were also tested for their influence on the histamine release from leukocytes of house dust mites-sensitive patients. Addition of TCS to B cell cultures from allergic donors induced a dose-dependent increase of the spontaneous IgE production without affecting the synthesis of IgG, IgM, and IgA. The potentiating activity of TCS was observed only in B cell cultures spontaneously producing IgE; TCS were still active on irradiated B cells. The maximal IgE-enhancing activity was observed when TCS were added at the onset of B cell cultures. The supernatants of T cells lysed at day 0 did not contain IgE-potentiating factors. The antigen-induced but not the spontaneous histamine release from leukocytes of house dust mite-sensitive patients was enhanced by pretreatment with TCS from allergic donors. The enhancing activities of TCS on IgE synthesis and on histamine release could be removed by absorption with IgE-Sepharose and subsequently recovered by elution with glycine buffer. The results indicate that T cells of patients with asthma spontaneously release IgE-binding factors capable of increasing both the spontaneous IgE synthesis by B cells and the antigen-induced histamine release.

Asthma↗
PubMed1987

Thromboxane A2 analogue induced coronary artery vasoconstriction in the rabbit.

Diffuse coronary artery vasoconstriction was provoked in the rabbit by a stable thromboxane A2 analogue, STA2 (9,11-epithio-11,12-methano thromboxane A2). Injection of 25 micrograms.kg-1 STA2 into the left main trunk caused complete occlusion of the left anterior descending artery and narrowing of the left circumflex artery. Two minutes after injection, however, the diameter of the coronary artery returned to the control value (n = 10). The right coronary artery was also temporarily occluded by an injection of 25 micrograms.kg-1 STA2. Left ventricular end diastolic pressure increased significantly, and ST segment elevation of the electrocardiogram occurred during vasoconstriction. The angiographic findings showed that the vasoconstriction in the coronary artery induced by STA2 was similar to the diffuse vasoconstriction seen clinically. Induction of the vasoconstriction by STA2 was prevented by the preadministration of 25 micrograms.kg-1 of either a calcium antagonist, diltiazem, or a thromboxane A2 receptor antagonist, ONO 3708 (n = 10). The relation of the calcium movement to this vasoconstriction was studied in vitro using the isolated left circumflex artery in the rabbit. STA2 (50 micrograms.litre-1 to 0.5 mg.litre-1) produced a concentration dependent contraction of helical strips of left circumflex artery. Diltiazem (50-100 g.litre-1) suppressed this contraction dose dependently. ONO 3708 (10 micrograms.litre-1 to 1 mg.litre-1) caused a significant rightward and downward shift of the dose-response curve.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1987

Modulation of IgE synthesis by IgE-binding factors released by T cells of asthmatic patients with elevated serum IgE.

The culture supernatants of unstimulated T cells (TCS) from asthmatic patients with elevated serum IgE were tested for IgE-binding factors (IgE-BFs) displaying the IgE-potentiating activity. The IgE-BFs were detected by their ability to inhibit the rosetting of RPMI 8866 cells with ox erythrocytes coupled with mouse monoclonal antibody (E-Mab) specific to Fc receptors for IgE (Fc epsilon R). TCS showing the rosette-inhibiting activity significantly enhanced the spontaneous IgE synthesis by B cells of allergic individuals. Interestingly, rosette-inhibiting factors could be removed by absorption with IgE-Sepharose from which they were subsequently eluated with acid buffer, indicating that the rosette inhibition was indeed mediated by IgE-BFs. In addition, such IgE-BFs had affinity for concanavalin A and lost their IgE-potentiating activity after treatment with trypsin and neuraminidase. In contrast, T cells treated with tunicamycin released IgE-suppressing factors capable of inhibiting the IgE-potentiating activity of TCS derived from untreated T cells. On the other hand, the culture supernatants from subpopulations depleted of Fc epsilon R+ T cells but not of Fc gamma R+ T cells contained neither rosette-inhibiting factors nor IgE-potentiating factors, suggesting that IgE-BFs were released by in vivo pre-activated Fc epsilon R+ T cells. With regard to circulating Fc epsilon R+ T cells determined by E-Mab, they were significantly higher in asthmatic patients with elevated serum IgE (0.77 +/- 0.15%) than in normal subjects (0.17 +/- 0.07%) in spite of a very small proportion of T cells bearing Fc epsilon R.

Asthma↗
PubMed1987

Effect of human interferon on different functions of human neutrophils and eosinophils.

The capacity of neutrophils treated with interferon to release peroxidase or superoxide anion was increased when the cells were stimulated with opsonized zymosan, while it was decreased in eosinophils. The effect of treatment with interferon was thought to be mediated by a change in expression of C3b receptors on the neutrophils or eosinophils. The production of a slow-reacting substance of anaphylaxis by eosinophils stimulated with opsonized zymosan or human IgG-coupled Sepharose 4B beads was markedly enhanced after incubation with interferon. Therefore it is suggested that interferon may play a role in the worsening of the condition in patients with bronchial asthma.

Asthma↗
PubMed1987

Heparin requirement in tissue-type plasminogen activator-induced experimental coronary thrombolysis: comparison with urokinase-induced coronary thrombolysis.

The requirement of heparin in experimental coronary thrombolysis induced by tissue-type plasminogen activator (t-PA) was studied in closed-chest dogs with one hour old coronary thrombi and compared with that in urokinase (UK)-induced coronary thrombolysis. Animals were divided into 5 treatment groups as follows: group 1 received intracoronary t-PA alone (1,000 IU/kg/min; n = 5), and if thrombolysis was not induced within 40 to 50 min, dogs then received an intravenous injection of heparin (300 U/kg) plus intracoronary t-PA; group 2 received intravenous heparin at first, and if thrombolysis was not induced within 10 min, dogs subsequently received intracoronary t-PA (n = 5); group 3 also received intravenous heparin at first, and if thrombolysis was not induced within 10 min, dogs subsequently received t-PA but intravenously, as compared with the groups administered by the intracoronary route (n = 6); group 4 received intracoronary UK alone (1,000 IU/kg/min; n = 6); group 5 received intravenous heparin at first, and if thrombolysis was not induced within 10 min, dogs subsequently received intracoronary UK (n = 5). Thrombolysis was confirmed angiographically. In group I, coronary thrombolysis could not be induced within 44 +/- 4 min by intracoronary t-PA alone, but it occurred in 8 +/- 4 min when administered in combination with heparin in all dogs. Heparin alone failed to elicit reperfusion within 10 min in group 2, 3 and 5. t-PA, however, induced successful reperfusion in 16 +/- 5 min (group 2) and in 23 +/- 6 min (group 3), respectively.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1987

Serum PGI2-regulating factors in acute myocardial infarction.

Human serum or plasma contains two factors which regulate PGI2 metabolism. The one is "PGI2-synthesis stimulating factor" which stimulates PGI2 synthesis in the vessel wall. The other is "PGI2-stabilizing factor" which stabilizes PGI2 in the blood. In the very early phase of acute myocardial infarction, the serum levels of these two factors were significantly reduced, which may be related to the thrombus formation in the coronary artery in acute myocardial infarction.

Blood Proteins↗
PubMed1987

Hemodynamic effect of oral TA-064 after dobutamine in congestive heart failure.

The hemodynamic effect of oral TA-064 (20 mg), a newly synthesized inotropic agent, was compared with that of intravenous dobutamine (5 micrograms/kg/min) in eight patients with congestive heart failure who had been treated with intravenous dobutamine, digitalis, diuretics, and prazosin. Hemodynamics was measured using a Swan-Ganz catheter during the pre-dobutamine control period, during dobutamine infusion period, during the pre-TA-064 control period and at 90 minutes after oral administration of TA-064. Stroke work index was increased and mean pulmonary capillary wedge pressure was decreased with TA-064 or dobutamine. Cardiac index and stroke index was increased by each drug, and pulmonary and systemic vascular resistances were decreased. Mean systemic arterial pressure, heart rate and pressure-rate product did not significantly change in comparison with the control level. In conclusion, TA-064 has a hemodynamic effect similar to that of dobutamine and may be useful as an oral substitute for dobutamine in patients with congestive heart failure after temporary management with dobutamine.

Administration, Oral↗
PubMed1987

Diffuse triple-vessel coronary artery spasm complicated by idioventricular rhythm and syncope.

A 70-year-old man presented with diffuse triple-vessel coronary arterial spasm accompanied by ST segment elevation in the inferior and anterior leads when the severity of pain moderated. At the beginning, he noted throat and chest pain followed by syncope. Atropine, norepinephrine, and lidocaine were administered therapeutically. The initial electrocardiogram showed an idioventricular rhythm without ST segment deviations, which made the prompt diagnosis of coronary arterial spasm difficult.

Aged↗